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Gastrointestinal Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Gareth Davies, Chris Black, Keeley Fairbrass
Treatment is with bile acid sequestering agents (e.g. colestyramine). Side effects include reduced absorption of fat-soluble vitamins and of many drugs, thus if used long-term, vitamin A and D supplements are recommended, and concomitant medication should be taken well before or after the colestyramine dose.
Do I Have IBS?
Published in Melissa G. Hunt, Aaron T. Beck, Reclaim Your Life From IBS, 2022
Melissa G. Hunt, Aaron T. Beck
One frequently overlooked cause of chronic diarrhea is bile acid. Bile acid is produced by the liver, stored in the gall bladder, and then secreted into the intestines where it plays a very important role in the digestion of fats and the regulation of cholesterol. In a healthy GI system, the liver produces the right amount, the gall bladder squirts the right amount into the upper part of the small intestine, where it does its thing, and then most of the excess bile acid is reabsorbed in the ileum, which is the last part of the small intestine, and thriftily returned to the liver for recirculation. A little escapes into the large intestine, where it is further transformed into secondary bile acid, and very small quantities are excreted in the stool every day. That’s if everything is working correctly. Unfortunately, there are several ways for this process to go wrong, and when it does, you end up with too much bile acid in the large intestine, which can cause chronic diarrhea, urgency, and even fecal incontinence.
Gut Microbiota—Specific Food Design
Published in Megh R. Goyal, Preeti Birwal, Santosh K. Mishra, Phytochemicals and Medicinal Plants in Food Design, 2022
Aparna V. Sudhakaran, Himanshi Solanki
Bile acids in the small intestine largely influence the digestion and absorption of dietary lipids. Chemically, the synthesis of primary bile acids takes place in the liver and secondary bile acids take place in the large intestine. Majority of primary bile acids (cholic acid and chenodeoxychlic acid) will be absorbed from Ileum for recycling in the liver. The remaining bile acids (1%–5%) reaching the colon will be modulated by the gut microbiota. The gut microflora regulates the bile acid synthesis as well as the conjugation of secondary bile acids (biotransformation). The secondary bile acids like deoxycholic acid have greater detergent properties thereby controlling the bacterial populations. The gut microbes have bile salt hydrolase (BSH) enzymes, which mediates the biotransformation of bile by hydrolyzing the glycol and tauro conjugates. Some of the genera reported to produce BSH are the Bacteroides, Bifidobacterium, Clostridium, Lactobacillus, and Listeria.
The level of serum total bile acid is related to atherosclerotic lesions, prognosis and gut Lactobacillus in acute coronary syndrome patients
Published in Annals of Medicine, 2023
Ting-Ting Liu, Jie Wang, Yan Liang, Xiao-Yuan Wu, Wen-Qing Li, Yu-Hang Wang, An-Ran Jing, Miao-Miao Liang, Li Sun, Jing Dou, Jing-Yu Liu, Yin Liu, Zhuang Cui, Jing Gao
As one of the main metabolites of cholesterol, bile acids play qualities of momentous roles in lipid metabolism, glucose metabolism and energy metabolism [1–3]. Bile acids are classified into primary and secondary bile acids. In the liver, primary bile acids are synthesized from cholesterol, while in the intestine, secondary bile acids are synthesized from primary bile acids as substrates by the intestinal microbiota. The entero-hepatic cycle – a persistent loop connecting bile acid secretion in the gut lumen, microbial transformation, ileal reabsorption and vascular transit through the portal circulation to the liver – is a link between the microbiota and the host [3]. Animal studies have shown that in the absence of hepatobiliary system disease, increased excretion of bile acids counteracted the cholesterol overload caused by a high-cholesterol diet and delayed atherosclerotic lesions [4]. Pharmacological studies have shown that bile acid chelators could reduce cholesterol levels in the blood, especially LDL cholesterol levels, in patients with various metabolic diseases [5,6]. Therefore, an imbalance of bile acid metabolism will lead to disorders of lipid metabolism, especially cholesterol metabolism, which will lead to the occurrence and progression of atherosclerosis [7,8].
Emerging drugs for hepatitis D
Published in Expert Opinion on Emerging Drugs, 2023
After the approval of the drug by the EMA, this treatment was applied to patients through early access programs (EAPs) in France, Italy, Germany, and Austria. In the French EAP BLV 2 mg/day monotherapy was given to 77 patients and BLV 2 mg/day + PegIFNα 180 µg/wk combination was given to 56 patients. HDV RNA decrease was −3.64 log IU/ml in the BLV monotherapy group at the end of 12th month, while it was −5.55 log IU/ml in the combination group. Similarly, virological response (at least 2 log decrease in HDV RNA level from baseline) was 52% vs 84% and 68% vs 94% at weeks 24 and 48, respectively. At the end of the 48th week, the rate of undetectable HDV RNA was found to be 39% and 85% and ALT normalization rates were 49% and 36%, with mono vs. combination treatment. Respectively, at the end of the 48th week. Similar to the phase II-III studies, no serious side effects were observed in the French EAP. Asymptomatic increase in bile acids was observed in almost all patients. Itching was not reported in any patient [80].
Mechanism of Huangqi–Honghua combination regulating the gut microbiota to affect bile acid metabolism towards preventing cerebral ischaemia–reperfusion injury in rats
Published in Pharmaceutical Biology, 2022
Kai Wang, Yue Chen, Jinyi Cao, Ruimin Liang, Yi Qiao, Likun Ding, Xiaojuan Yang, Zhifu Yang
Gut microbiota is a complex community of microorganisms and plays a major role in health and disease (Adak and Khan 2019; Angelucci et al. 2019). Gut microbiota regulates the human digestive, metabolic, inflammatory, and immune functions (Cryan et al. 2019). A close relationship exists between gut microbiota and ischaemic stroke. Ischaemic stroke alters the composition of the intestinal microbiota, and intestinal microbiota can affect the occurrence and development of ischaemic stroke (Nam 2019). Alteration of gut microbiota can protect from cerebral ischaemia-induced brain injury. Intestinal flora can alter the immune homeostasis of the small intestine, which leads to an increase in Treg cells and a reduction in interleukin-17 (IL-17) positive γδT or T helper cells 17 (Th17) through altered dendritic cell activity, which increases IL-10 and reducing IL-17, thereby reducing systemic inflammation after acute ischaemic stroke and exerting neuroprotective effects (Benakis et al. 2016). Intestinal flora is involved in the synthesis, metabolism, and signal transduction of bile acids. Bile acids play an important role in regulating various pathophysiological processes such as lipid, glucose stability, inflammatory response, intestinal microflora structure and growth, and the occurrence and development of atherosclerosis, obesity, cholestasis, and other diseases (Li and Chiang 2014). Therefore, we determined the relationship between the intestinal flora and bile acid metabolism changes in ischaemic stroke from a multi-group approach, which is particularly important for understanding the effect of drug treatment.